The Claim
Thyroid hormone induces rapid intracellular calcium mobilization in human HeLa and mouse C2C12 cells, and this calcium mobilization is necessary for the subsequent activation of AMPK and stimulation of fatty acid oxidation, as evidenced by the suppression of AMPK activation and fatty acid oxidation following treatment with the calcium chelator BAPTA.
What the research says
Supports is higher
Support is ahead, but a single strong opposing study can change this.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
Thyroid hormone triggers a rapid increase in calcium inside human and mouse muscle cells, and this calcium increase is required for activating AMPK and increasing the breakdown of fatty acids.
See the scientific wording
Thyroid hormone induces rapid intracellular calcium mobilization in human HeLa and mouse C2C12 cells, which is necessary for the subsequent activation of AMPK and stimulation of fatty acid oxidation, as demonstrated by suppression of these effects with the calcium chelator BAPTA.
Thyroid hormone binds to receptors on the cell, causing calcium to be released from internal stores. This calcium surge activates a protein that turns on AMPK, which then shuts down a blocker of fat burning, allowing fatty acids to enter mitochondria and be burned for energy.
What the research says
1 studyThyroid hormone tells cells to start burning fat for energy, but it needs a quick calcium signal to do it. When scientists blocked that calcium signal, the fat-burning stopped — proving the signal is necessary.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.